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Gastrointestinal Bleeding in Acute Ischemic Stroke: Recent Trends from the Fukuoka Stroke Registry

机译:急性缺血性中风的胃肠道出血:福冈中风病登记处的最新趋势

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Background: Gastrointestinal (GI) hemorrhage is a potentially serious complication of acute stroke, but its incidence appears to be decreasing. The aim of this study was to elucidate the etiology of GI bleeding and its impact on clinical outcomes in patients with acute ischemic stroke in recent years. Methods: Using the database of the Fukuoka Stroke Registry, 6,529 patients with acute ischemic stroke registered between June 2007 and December 2012 were included in this study. We recorded clinical data including any previous history of peptic ulcer, prestroke drug history including the use of antiplatelets, anticoagulants, steroids and nonsteroidal anti-inflammatory drugs (NSAIDs), and poststroke treatment with suppressing gastric acidity. GI bleeding was defined as any episode of hematemesis or melena on admission or during hospitalization. The cause and origin of bleeding were diagnosed endoscopically. Logistic regression analysis was used to identify risk factors for GI bleeding and its influence on deteriorating neurologic function, death, and poor outcome. Results: GI bleeding occurred in 89 patients (1.4%) under the condition that 66% of the total patients received acid-suppressing agents after admission. Multivariate analysis revealed that GI bleeding was associated with the absence of dyslipidemia (p = 0.03), a previous history of peptic ulcer (p < 0.001), and the severity of baseline neurologic deficit (p = 0.002) but not with antiplatelet drugs, anticoagulants, and NSAIDs. The source was the upper GI tract in 51% of the cases; causes included peptic ulceration (28%) and malignancies (12%), and other or unidentified causes accounted for 60%. GI bleeding mostly occurred within 1 week after stroke onset. Hemoglobin concentration fell by a median value of 2.5 g/dl in patients with GI bleeding. Among them, 28 patients underwent blood transfusion (31.5%). After adjustment for confounding factors, GI bleeding was independently associated with neurologic deterioration (OR 3.9, 95% CI 2.3-6.6, p < 0.001), in-hospital death (OR 6.1, 95% CI 3.1-12.1, p < 0.001), and poor outcome at 3 months (OR 6.8, 95% CI 3.7-12.7, p < 0.001). These associations were significant irrespective of whether patients underwent red blood cell transfusion. Conclusions: GI bleeding infrequently occurred in patients with acute ischemic stroke, which was mostly due to etiologies other than peptic ulcer. GI bleeding was associated with poor clinical outcomes including neurologic deterioration, in-hospital mortality, and poor functional outcome.
机译:背景:胃肠道(GI)出血是急性中风的潜在严重并发症,但其发生率似乎正在下降。这项研究的目的是阐明近年来胃肠道出血的病因及其对急性缺血性中风患者临床预后的影响。方法:使用福冈中风病登记处的数据库,纳入2007年6月至2012年12月之间登记的6,529例急性缺血性中风患者。我们记录了临床数据,包括以前的消化性溃疡病史,中风药物史,包括使用抗血小板药,抗凝剂,类固醇和非甾体抗炎药(NSAIDs)以及中风后抑制胃酸的治疗。胃肠道出血定义为入院时或住院期间出现的任何呕血或黑便。内镜诊断出血的原因和起源。逻辑回归分析用于确定胃肠道出血的危险因素及其对神经功能恶化,死亡和不良结局的影响。结果:89例患者(1.4%)发生胃肠道出血,条件是入院后总患者中有66%接受了抑酸剂。多变量分析表明,胃肠道出血与血脂异常的缺乏(p = 0.03),先前有消化性溃疡病史(p <0.001)和基线神经功能缺损的严重程度(p = 0.002)有关,而与抗血小板药物和抗凝剂无关和NSAID。在51%的病例中,源是上消化道。原因包括消化性溃疡(28%)和恶性肿瘤(12%),其他或不明原因占60%。胃肠道出血多发生在中风发作后1周内。胃肠道出血患者的血红蛋白浓度下降了2.5 g / dl。其中28例患者输血(31.5%)。调整混杂因素后,胃肠道出血与神经系统恶化(OR 3.9,95%CI 2.3-6.6,p <0.001),院内死亡(OR 6.1,95%CI 3.1-12.1,p <0.001)独立相关,且3个月时的预后较差(OR 6.8,95%CI 3.7-12.7,p <0.001)。无论患者是否进行了红细胞输注,这些关联都是显着的。结论:急性缺血性卒中患者很少发生胃肠道出血,这主要是由于消化性溃疡以外的病因引起的。胃肠道出血与不良的临床预后相关,包括神经系统恶化,住院死亡率和不良的功能预后。

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